Chapter 13. Memory, Learning, and Development
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|By Lisa Marshall Is Alzheimer's disease an acquired form of Down syndrome? When neurobiologist Huntington Potter first posed the question in 1991, Alzheimer's researchers were skeptical. They were just beginning to explore the causes of the memory-robbing neurological disease. Scientists already knew that by age 40, nearly 100 percent of patients with Down syndrome, who have an extra copy of chromosome 21, had brains full of beta-amyloid peptide—the neuron-strangling plaque that is a hallmark of Alzheimer's. They also knew that the gene that codes for that protein lives on chromosome 21, suggesting that people acquire more plaque because they get an extra dose of the peptide. Potter, though, suggested that if people with Down syndrome develop Alzheimer's because of an extra chromosome 21, healthy people may develop Alzheimer's for the same reason. A quarter of a century later mounting evidence supports the idea. “What we hypothesized in the 1990s and have begun to prove is that people with Alzheimer's begin to make molecular mistakes and generate cells with three copies of chromosome 21,” says Potter, who was recently appointed director of Alzheimer's disease research at the University of Colorado School of Medicine, with the express purpose of studying Alzheimer's through the lens of Down syndrome. He is no longer the only one exploring the link. In recent years dozens of studies have shown Alzheimer's patients possess an inordinate amount of Down syndrome–like cells. One 2009 study by Russian researchers found that up to 15 percent of the neurons in the brains of Alzheimer's patients contained an extra copy of chromosome 21. Others have shown Alzheimer's patients have 1.5 to two times as many skin and blood cells with the extra copy as healthy controls. Potter's own research in mice suggests a vicious cycle: when normal cells are exposed to the beta-amyloid peptide, they tend to make mistakes when dividing, producing more trisomy 21 cells, which, in turn, produce more plaque. In August, Potter and his team published a paper in the journal Neurobiology of Aging describing why those mistakes may occur: the inhibition of a specific enzyme. © 2014 Scientific American
Link ID: 19771 - Posted: 06.25.2014
By Gary Stix Tony Zador: The human brain has 100 billion neurons, a mouse brain has maybe 100 million. What we’d really like to understand is how we go from a bunch of neurons to thought, feelings, behavior. We think that the key is to understand how the different neurons are connected to one another. So traditionally there have been a lot of techniques for studying connectivity but at a fairly crude level. We can, for instance, tell that a bunch of neurons here tend to be connected to a bunch of neurons there. There are also techniques for looking at how single neurons are connected but only for individual links between those neurons. What we would love to be able to do is to tell how every single neuron in the brain is connected to every single other neuron in the brain. So if you wanted to navigate through the United States, one of the most useful things you could have is a roadmap. It wouldn’t tell you everything about the United States, but it would be very hard to get around without a complete roadmap of the country. We need something like that for the brain. Zador: Traditionally the way people study connectivity is as a branch of microscopy. Typically what people do is they use one method or another to label a neuron and then they observe that neuron at some level of resolution. But the challenge that’s at the core of all the microscopy techniques is that neurons can extend long distances. That might be millimeters in a mouse brain or, in fact, in a giraffe brain, there are neurons that go all the way from the brain to its foot, which can be over 15 feet. Brain cells are connected with one another at structures called synapses, which are below the resolution of light microscopy. That means that if you really want to understand how one neuron is connected to another, you need to resolve the synapse, which requires electron microscopy. You have to take incredibly thin sections of brain and then image them. © 2014 Scientific American
|By Lindsey Konkel and Environmental Health News Babies whose moms lived within a mile of crops treated with widely used pesticides were more likely to develop autism, according to new research. The study of 970 children, born in farm-rich areas of Northern California, is part of the largest project to date that is exploring links between autism and environmental exposures. The University of California, Davis research – which used women’s addresses to determine their proximity to insecticide-treated fields – is the third project to link prenatal pesticide exposures to autism and related disorders. “The weight of evidence is beginning to suggest that mothers’ exposures during pregnancy may play a role in the development of autism spectrum disorders,” said Kim Harley, an environmental health researcher at the University of California, Berkeley who was not involved in the new study. One in every 68 U.S. children has been identified with an autism spectrum disorder—a group of neurodevelopmental disorders characterized by difficulties with social interactions, according to the Centers for Disease Control and Prevention. “This study does not show that pesticides are likely to cause autism, though it suggests that exposure to farming chemicals during pregnancy is probably not a good thing,” said Dr. Bennett Leventhal, a child psychiatrist at University of California, San Francisco who studies autistic children. He did not participate in the new study. The biggest known contributor to autism risk is having a family member with it. Siblings of a child with autism are 35 times more likely to develop it than those without an autistic brother or sister, according to the National Institutes of Health. © 2014 Scientific American
By DOUGLAS QUENQUA When it comes to forming memories that involve recalling a personal experience, neuroscientists are of two minds. Some say that each memory is stored in a single neuron in a region of the brain called the hippocampus. But a new study is lending weight to the theory of neuroscientists who believe that every memory is spread out, or distributed, across many neurons in that part of the brain. By watching patients with electrodes in their brains play a memory game, researchers found that each such memory is committed to cells distributed across the hippocampus. Though the proportion of cells responsible for each memory is small (about 2 percent of the hippocampus), the absolute number is in the millions. So the loss of any one cell should not have a noticeable effect on memory or mental acuity, said Peter N. Steinmetz, a research neurologist at the Dignity Health Barrow Neurological Institute in Phoenix and senior author of the study. “The significance of losing one cell is substantially reduced because you’ve got this whole population that’s turning on” when you access a memory, he said. The findings also suggest that memory researchers “need to use techniques that allow us to look at the whole population of neurons” rather than focus on individual cells. The patients in the study, which is published in Proceedings of the National Academy of Sciences, first memorized a list of words on a computer screen, then viewed a second list that included those words and others. When asked to identify words they had seen earlier, the patients displayed cell-firing activity consistent with the distributed model of memory. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 19763 - Posted: 06.24.2014
|By Tori Rodriguez One of the most devastating aspects of Alzheimer's is its effect on patients' ability to recall life events. Several studies have found that music helps to strengthen these individuals' autobiographical memories, and a paper in the November 2013 Journal of Neurolinguistics builds on these findings by exploring the linguistic quality of those recollections. Researchers instructed 18 patients with Alzheimer's and 18 healthy control subjects to tell stories from their lives in a silent room or while listening to the music of their choice. Among the Alzheimer's patients, the music-cued stories contained a greater number of meaningful words, were more grammatically complex and conveyed more information per number of words. Music may enhance narrative memories because “music and language processing share a common neural basis,” explains study co-author Mohamad El Haj of Lille University in France. © 2014 Scientific American
Link ID: 19762 - Posted: 06.24.2014
By Adam Carter, CBC News Women who take antidepressants when they’re pregnant could unknowingly predispose their kids to type 2 diabetes and obesity later on in life, new research out of McMaster University suggests. The study, conducted by associate professor of obstetrics and gynecology Alison Holloway and PhD student Nicole De Long, found a link between the antidepressant fluoxetine and increased risk of obesity and diabetes in children. Holloway cautions that this is not a warning for all pregnant women to stop taking antidepressants, but rather to start a conversation about prenatal care and what works best on an individual basis. “There are a lot of women who really need antidepressants to treat depression. This is what they need,” Holloway told CBC. “We’re not saying you should necessarily take patients off antidepressants because of this — but women should have this discussion with their caregiver.” “Obesity and Type 2 diabetes in children is on the rise and there is the argument that it is related to lifestyle and availability of high calorie foods and reduced physical activity, but our study has found that maternal antidepressant use may also be a contributing factor to the obesity and diabetes epidemic.” According to a study out of Memorial University in St. John's, obesity rates in Canada have tripled between 1985 and 2011. Canada also ranks poorly when it comes to its overall number of cases of diabetes, according to international report from the Organization for Economic Co-operation and Development, released last year. © CBC 2014
By Elizabeth Norton A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood. That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. "Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn't seem to be there before, if only for a short time during a fever or other stress" says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders. Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child. As a specialist in the cell's life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay "higher up" in the cell's metabolism. © 2014 American Association for the Advancement of Science.
Link ID: 19749 - Posted: 06.19.2014
by Lauren Hitchings Our brain's ability to rapidly interpret and analyse new information may lie in the musical hum of our brainwaves. We continuously take in information about the world but establishing new neural connections and pathways – the process thought to underlie memory formation – is too slow to account for our ability to learn rapidly. Evan Antzoulatos and Earl Miller at the Massachusetts Institute of Technology decided to see if brainwaves – the surges of electricity produced by individual neurons firing en masse – play a role. They used EEG to observe patterns of electrical activity in the brains of monkeys as they taught the animals to categorise patterns of dots into two distinct groups. At first, they memorised which dots went where, but as the task became harder, they shifted to learning the rules that defined the categories. Humming brainwaves The researchers found that, initially, brainwaves of different frequencies were being produced independently by the prefrontal cortex and the striatum – two brain regions involved in learning. But as the monkeys made sense of the game, the waves began to synchronise and "hum" at the same frequency – with each category of dots having its own frequency. Miller says the synchronised brainwaves indicate the formation of a communication circuit between the two brain regions. He believes this happens before anatomical changes in brain connections take place, giving our minds time to think through various options when presented with new information before the right one gets laid down as a memory. Otherwise, the process is too time-consuming to account for the flexibility and speed of the human mind, says Miller. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 19746 - Posted: 06.19.2014
by Bethany Brookshire When a cartoon character gets an idea, you know it. A lightbulb goes on over Wile E. Coyote’s head, or a ding sounds as Goofy puts two and two together. While the lightbulb and sound effects are the stuff of cartoons, scientists can, in a way, watch learning in action. In a new study, a learning task in rats was linked to increases in activity patterns in groups of brain cells. The results might help scientists pin down what learning looks like at the nerve cell level, and give us a clue about how memories are made. Different areas of the brain communicate with each other, transferring information from one area to another for processing and interpretation. Brain cell meets brain cell at connections called synapses. But to transfer information between areas often takes more than one neuron firing a lonely signal. It takes cortical oscillations — networks of brain cells sending electrical signals in concert — over and over again for a message to transmit from one brain area to another. Changes in electrical fields increase the probability that neurons in a population will fire. These cortical oscillations are like a large crowd chanting. Not all voices may be yelling at once, some people may be ahead or behind, some may even be whispering, but you still hear an overwhelming “USA! USA!” Cortical oscillations can occur within a single brain area, or they can extend from one area to another. “The oscillation tells you what the other brain area is likely to ‘see’ when it gets that input,” explains Leslie Kay, a neuroscientist at the University of Chicago. Once the receiving area ‘sees’ the incoming oscillation, it may synchronize its own population firing, joining in the chant. “A synchronized pattern of oscillations in two separate brain regions serves to communicate between the two regions,” says Kei Igarashi, a neuroscientist at the Norwegian University of Science and Technology in Trondheim. © Society for Science & the Public 2000 - 2013
Keyword: Learning & Memory
Link ID: 19742 - Posted: 06.17.2014
As the popularity of soccer grows among children, doctors and researchers say the dangers of concussions need to be taken more seriously in the sport. When researchers at St. Michael's Hospital in Toronto reviewed the evidence on concussions and heading in soccer this winter, they found a higher incidence of concussions among females than males playing the world's most popular sport. Doctors warn that heading — purposely using the head to control and hit the ball — is a unique aspect of the beautiful game that needs more attention. Heading the ball isn’t necessarily going to cause an overt concussion with symptoms, but the accumulation of those impacts over time could cause difficulties with thinking, concentration and memory, said study author Monica Maher, a graduate student at the University of Toronto, and a former soccer goalkeeper. Maher doesn't want people to stop playing soccer or stop heading the ball. She does suggest limits on head exposure in younger children and padding on goal posts to prevent injury to the youngest players. Dr. David Robinson, a sports medicine physician at McMaster University in Hamilton, sees 10 to 15 concussions a week, including many related to soccer. "It's not a stretch to think that these chronic subconcussive blows may be softening the brain, injuring the brain over time," Robinson said. He calls it a step forward that balls are becoming lighter for young people. He reminds parents and coaches that if a concussion is suspected, it's best to remove an athlete from play. As for the differences in injury rates between males and females, Maher pointed to a few potential explanations: © CBC 2014
Virginia Morell Teaching isn’t often seen in animals other than humans—and it’s even more difficult to demonstrate in animals living in the wild rather than in a laboratory setting. But researchers studying the Australian superb fairy-wren (Malurus cyaneus) in the wild think the small songbirds (a male is shown in the photo above) practice the behavior. They regard a female fairy-wren sitting on her nest and incubating her eggs as the teacher, and her embryonic chicks as her pupils. She must teach her unhatched chicks a password—a call they will use after emerging to solicit food from their parents; the better they learn the password, the more they will be fed. Since 1992, there’s been a well-accepted definition of teaching that consists of three criteria. First, the teacher must modify his or her behavior in the presence of a naive individual—which the birds do; the mothers increase their teaching (that is, the rate at which they make the call) when their chicks are in a late stage of incubation. Second, there must be a benefit to the pupil, which there clearly is. Scientists reported online yesterday in Behavioral Ecology that the fairy-wrens also pass the third criteria: There must be a cost to the teacher. And for the small birds, there can be a hefty price to pay. The more often a female repeats the password, the more likely she is to attract a parasitical cuckoo, which will sneak in and lay its eggs in her nest. From careful field observations, the scientists discovered that at nests that were parasitized, the females had recited their password 20 times an hour. But at nests that were not parasitized, the females had called only 10 times per hour. Superb fairy-wrens thus join a short but growing list of animal-teachers, such as rock ants, meerkats, and pied babblers. © 2014 American Association for the Advancement of Science.
Associated Press In one of the most ambitious attempts yet to thwart Alzheimer's disease, a major study got under way Monday to see if an experimental drug can protect healthy seniors whose brains harbor silent signs that they're at risk. Scientists plan to eventually scan the brains of thousands of older volunteers in the U.S., Canada and Australia to find those with a sticky build-up believed to play a key role in development of Alzheimer's - the first time so many people without memory problems get the chance to learn the potentially troubling news. Having lots of that gunky protein called beta-amyloid doesn't guarantee someone will get sick. But the big question: Could intervening so early make a difference for those who do? "We have to get them at the stage when we can save their brains," said Dr. Reisa Sperling of Boston's Brigham and Women's Hospital and Harvard Medical School, who is leading the huge effort to find out. Researchers are just beginning to recruit volunteers, and on Monday, a Rhode Island man was hooked up for an IV infusion at Butler Hospital in Providence, the first treated. Peter Bristol, 70, of Wakefield, R.I., figured he was at risk because his mother died of Alzheimer's and his brother has it. "I felt I needed to be proactive in seeking whatever therapies might be available for myself in the coming years," said Bristol, who said he was prepared when a PET scan of his brain showed he harbored enough amyloid to qualify for the research. "Just because I have it doesn't mean I'm going to get Alzheimer's," he stressed. But Bristol and his wife are "going into the situation with our eyes wide open." He won't know until the end of what is called the A4 Study - it stands for Anti-Amyloid Treatment in Asymptomatic Alzheimer's - whether he received monthly infusions of the experimental medicine, Eli Lilly & Co.'s solanezumab, or a dummy drug. © 2014 Hearst Communications, Inc.
Link ID: 19717 - Posted: 06.10.2014
by Ashley Yeager Being put under anesthesia as an infant may make it harder for a person to recall details or events when they grow older. Previous studies on animals had shown that anesthesia impairs parts of the brain that help with recollection. But it was not clear how this type of temporary loss of consciousness affected humans. Comparing the memory of 28 children ages 6 to 11 who had undergone anesthesia as infants to 28 children similar in age who had not been put under suggests that the early treatment impairs recollection later in life, researchers report June 9 in Neuropsychopharmacology. The team reported similar results for a small study on rats and notes that early anesthesia did not appear to affect the children's familiarity with objects and events or their IQ. © Society for Science & the Public 2000 - 2013.
by Laura Sanders Transplanted cells can flourish for over a decade in the brain of a person with Parkinson’s disease, scientists write in the June 26 Cell Reports. Finding that these cells have staying power may encourage clinicians to pursue stem cell transplants, a still-experimental way to counter the brain deterioration that comes with Parkinson’s. Penelope Hallett of Harvard University and McLean Hospital in Belmont, Mass., and colleagues studied postmortem brain tissue from five people with advanced Parkinson’s. The five had received stem cell transplants between four and 14 years earlier. In all five people’s samples, neurons that originated from the transplanted cells showed signs of good health and appeared capable of sending messages with the brain chemical dopamine, a neurotransmitter that Parkinson’s depletes. Results are mixed about whether these transplanted cells are a good way to ease Parkinson’s symptoms. Some patients have shown improvements after the new cells stitched themselves into the brain, while others didn’t benefit from them. The cells can also cause unwanted side effects such as involuntary movements. P. J. Hallett et al. Long-term health of dopaminergic neuron transplants in Parkinson’s disease patients. Cell Reports. Vol. 7, June 26, 2014. doi: 10.1016/j.celrep.2014.05.027. © Society for Science & the Public 2000 - 2013
by Moheb Costandi Rest easy after learning a new skill. Experiments in mice suggest that a good night's sleep helps us lay down memories by promoting the growth of new connections between brain cells. Neuroscientists believe that memory involves the modification of synapses, which connect brain cells, and numerous studies published over the past decade have shown that sleep enhances the consolidation of newly formed memories in people. But exactly how these observations were related was unclear. To find out, Wenbiao Gan of the Skirball Institute of Biomolecular Medicine at New York University Medical School and his colleagues trained 15 mice to run backwards or forwards on a rotating rod. They allowed some of them to fall asleep afterwards for 7 hours, while the rest were kept awake. The team monitored the activity and microscopic structure of the mice's motor cortex, the part of the brain that controls movement, through a small transparent "window" in their skulls. This allowed them to watch in real time how the brain responded to learning the different tasks. Sprouting spines They found that learning a new task led to the formation of new dendritic spines – tiny structures that project from the end of nerve cells and help pass electric signals from one neuron to another – but only in the mice left to sleep. This happened during the non-rapid eye movement stage of sleep. Each task caused a different pattern of spines to sprout along the branches of the same motor cortex neurons. © Copyright Reed Business Information Ltd.
By Sadie Dingfelder Want to become famous in the field of neuroscience? You could go the usual route, spending decades collecting advanced degrees, slaving away in science labs and publishing your results. Or you could simply fall victim to a freak accident. The stars of local science writer Sam Kean’s new book, “The Tale of the Dueling Neurosurgeons,” (which he’ll discuss Saturday at Politics and Prose) took the latter route. Be it challenging the wrong guy to a joust, spinning out on a motorcycle, or suffering from a stroke, these folks sustained brain injuries with bizarre and fascinating results. One man, for instance, lost the ability to identify different kinds of animals but had no trouble naming plants and objects. Another man lost his short-term memory. The result? A diary filled with entries like: “I am awake for the very first time.” “Now, I’m really awake.” “Now, I’m really, completely awake.” Unfortunate mishaps like these have advanced our understanding of how the gelatinous gray mass that (usually) stays hidden inside our skulls gives rise to thoughts, feelings and ideas, Kean says. “Traditionally, every major discovery in the history of neuroscience came about this way,” he says. “We had no other way of looking at the brain for centuries and centuries, because we didn’t have things like MRI machines.” Rather than covering the case studies textbook-style, Kean provides all the gory details. Consider Phineas Gage. You may remember from Psych 101 that Gage, a railroad worker, survived having a metal rod launched through his skull. You might not know, however, that one doctor “shaved Gage’s scalp and peeled off the dried blood and gelatinous brains. He then extracted skull fragments from the wound by sticking his fingers in from both ends, Chinese-finger-trap-style,” as Kean writes in his new book. © 1996-2014 The Washington Post
By Jenny Graves The claim that homosexual men share a “gay gene” created a furor in the 1990s. But new research two decades on supports this claim – and adds another candidate gene. To an evolutionary geneticist, the idea that a person’s genetic makeup affects their mating preference is unsurprising. We see it in the animal world all the time. There are probably many genes that affect human sexual orientation. But rather than thinking of them as “gay genes,” perhaps we should consider them “male-loving genes.” They may be common because these variant genes, in a female, predispose her to mate earlier and more often and to have more children. Likewise, it would be surprising if there were not “female-loving genes” in lesbian women that, in a male, predispose him to mate earlier and have more children. We can detect genetic variants that produce differences between people by tracking traits in families that display differences. Patterns of inheritance reveal variants of genes (called “alleles”) that affect normal differences, such as hair color, or disease states, such as sickle cell anemia. Quantitative traits, such as height, are affected by many different genes, as well as environmental factors. It’s hard to use these techniques to detect genetic variants associated with male homosexuality partly because many gay men prefer not to be open about their sexuality. It is even harder because, as twin studies have shown, shared genes are only part of the story. Hormones, birth order and environment play roles, too.
Laura Spinney One day in 1991, neurologist Warren Strittmatter asked his boss to look at some bewildering data. Strittmatter was studying amyloid-β, the main component of the molecular clumps found in the brains of people with Alzheimer's disease. He was hunting for amyloid-binding proteins in the fluid that buffers the brain and spinal cord, and had fished out one called apolipoprotein E (ApoE), which had no obvious connection with the disease. Strittmatter's boss, geneticist Allen Roses of Duke University in Durham, North Carolina, immediately realized that his colleague had stumbled across something exciting. Two years earlier, the group had identified a genetic association between Alzheimer's and a region of chromosome 19. Roses knew that the gene encoding ApoE was also on chromosome 19. “It was like a lightning bolt,” he says. “It changed my life.” In humans, there are three common variants, or alleles, of the APOE gene, numbered 2, 3 and 4. The obvious step, Roses realized, was to find out whether individual APOE alleles influence the risk of developing Alzheimer's disease. The variants can be distinguished from one another using a technique called the polymerase chain reaction (PCR). But Roses had little experience with PCR, so he asked the postdocs in his team to test samples from people with the disease and healthy controls. The postdocs refused: they were busy hunting for genes underlying Alzheimer's, and APOE seemed an unlikely candidate. The feeling in the lab, recalls Roses, was that “the chief was off on one of his crazy ideas”. Roses then talked to his wife, Ann Saunders, a mouse geneticist who was skilled at PCR. She had just given birth to their daughter and was on maternity leave, so they struck a deal. “She did the experiments while I held the baby,” he says. Within three weeks, they had collected the data that would fuel a series of landmark papers showing that the APOE4 allele is associated with a greatly increased risk of Alzheimer's disease1. © 2014 Nature Publishing Group,
By Charles Q. Choi Scientists have found a kind of brain cell in mice that can instruct stem cells to start making more neurons, according to a new study. In addition, they found that electrical signals could trigger this growth in rodents, raising the intriguing possibility that devices could one day help the human brain repair itself. The study appears in the journal Nature Neuroscience. We knew the brain can generate new neurons, a process known as neurogenesis, via neural stem cells. And neuroscientists knew these stem cells got their instructions from a variety of sources from chemicals in the bloodstream, for instance, and from cells in the structures that hold the cerebrospinal fluid that cushion the brain. Earlier research had suggested brain cells might also be able to command these stem cells to create neurons. Neuroscientist Chay Kuo at the Duke University School of Medicine in Durham, N.C., and his colleagues have now discovered such cells in mice. "It's really cool that the brain can tell stem cells to make more neurons," Kuo says. To begin their experiments, the researchers tested how well a variety of neurotransmitters performed at spurring mouse neural stem cells to produce new neurons; they found that a compound known as acetylcholine performed best. The team then discovered a previously unknown type of neuron that produces an enzyme needed to make acetylcholine. These neurons are found in a part of the adult mouse brain known as the subventricular zone, where neurogenesis occurs. ©2014 Hearst Communication, Inc
Link ID: 19694 - Posted: 06.05.2014
Ewen Callaway By controlling rats' brain cells they had genetically engineered to respond to light, researchers were able to create fearful memories of events that never happened — and then to erase those memories again. Neuroscientists can breathe a collective sigh of relief. Experiments have confirmed a long-standing theory for how memories are made and stored in the brain. Researchers have created and erased frightening associations in rats' brains using light, providing the most direct demonstration yet that the strengthening and weakening of connections between neurons is the basis for memory. “This is the best evidence so far available, period,” says Eric Kandel, a neuroscientist at Columbia University in New York. Kandel, who shared the 2000 Nobel Prize in Physiology or Medicine for his work unravelling the molecular basis of memory, was not involved in the latest study, which was published online in Nature1 on 1 June. In the 1960s and 1970s, researchers in Norway noticed a peculiar property of brain cells. Repeatedly delivering a burst of electricity to a neuron in an area of the brain known as the hippocampus seemed to boost the cell’s ability to talk to a neighbouring neuron. These communiqués occur across tiny gaps called synapses, which neurons can form with thousands of other nerve cells. The process was called long-term potentiation (LTP), and neuroscientists suspected that it was the physical basis of memory. The hippocampus, they realized, was important for forming long-term memories, and the long-lasting nature of LTP hinted that information might be stored in a neural circuit for later recall. © 2014 Nature Publishing Group,